Resveratrol Attenuates the Blood-Brain Barrier Dysfunction by Regulation of the MMP-9/TIMP-1 Balance after Cerebral Ischemia Reperfusion in Rats

Wei, Haidong; Wang, Shiquan; Zhen, Luming; Yang, Qianzi; Wu, Zhixin; Li, Xiaoming; Lv, Jianrui; Xiong, Lize; Xue, Renyu

doi:10.1007/s12031-014-0441-1

Cited by 64 publications

(48 citation statements)

References 37 publications

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“…Resveratrol has been shown to cross BBB, and regulate expression of MMPs, reduce pericyte loss, maintain integrity of BBB, and promote Aβ clearance [224–226]. Treatment with resveratrol completely reversed diabetes-induced vascular dysfunction by reducing capillary leakage, pericyte degeneration, and VEGF protein expression in the murine retina [227].…”

Section: Vasculoprotective Approachesmentioning

confidence: 99%

Neurovascular dysfunction and neurodegeneration in dementia and Alzheimer's disease

Nelson

Sweeney

Sagare

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

437

423

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Vascular insults can initiate a cascade of molecular events leading to neurodegeneration, cognitive impairment and dementia. Here, we review the cellular and molecular mechanisms in cerebral blood vessels and the pathophysiological events leading to cerebral blood flow dysregulation and disruption of the neurovascular unit and the blood-brain barrier, which all may contribute to the onset and progression of dementia and Alzheimer’s disease (AD). Particularly, we examine the link between neurovascular dysfunction and neurodegeneration including the effects of AD genetic risk factors on cerebrovascular functions and clearance of Alzheimer’s amyloid-β peptide toxin, and the impact of vascular risk factors, environment and lifestyle on cerebral blood vessels, which in turn may affect synaptic, neuronal and cognitive functions. Finally, we examine potential experimental treatments for dementia and AD based on the neurovascular model, and discuss some critical questions to be addressed by future studies.

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Section: Vasculoprotective Approachesmentioning

confidence: 99%

Neurovascular dysfunction and neurodegeneration in dementia and Alzheimer's disease

Nelson

Sweeney

Sagare

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

437

423

View full text Add to dashboard Cite

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“…Aged garlic extract protects against BBB disruption caused by a high saturated fatty acid diet in mice [331]. Resveratrol, a component of grape and red fruit skins, and red wine [332], maintains the integrity of the BBB after cerebral ischemia reperfusion in rats [333]…”

Section: Components Of the Mediterranean Dietmentioning

confidence: 99%

Genetic, Transcriptome, Proteomic, and Epidemiological Evidence for Blood-Brain Barrier Disruption and Polymicrobial Brain Invasion as Determinant Factors in Alzheimer’s Disease

Carter

2017

ADR

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Diverse pathogens are detected in Alzheimer’s disease (AD) brains. A bioinformatics survey showed that AD genome-wide association study (GWAS) genes (localized in bone marrow, immune locations and microglia) relate to multiple host/pathogen interactomes (Candida albicans, Cryptococcus neoformans, Bornavirus, Borrelia burgdorferri, cytomegalovirus, Ebola virus, HSV-1, HERV-W, HIV-1, Epstein-Barr, hepatitis C, influenza, Chlamydia pneumoniae, Porphyrymonas gingivalis, Helicobacter pylori, Toxoplasma gondii, Trypanosoma cruzi). These interactomes also relate to the AD hippocampal transcriptome and to plaque or tangle proteins. Upregulated AD hippocampal genes match those upregulated by multiple bacteria, viruses, fungi, or protozoa in immunocompetent cells. AD genes are enriched in GWAS datasets reflecting pathogen diversity, suggesting selection for pathogen resistance, as supported by the old age of AD patients, implying resistance to earlier infections. APOE4 is concentrated in regions of high parasitic burden and protects against childhood tropical infections and hepatitis C. Immune/inflammatory gain of function applies to APOE4, CR1, and TREM2 variants. AD genes are also expressed in the blood-brain barrier (BBB), which is disrupted by AD risk factors (age, alcohol, aluminum, concussion, cerebral hypoperfusion, diabetes, homocysteine, hypercholesterolemia, hypertension, obesity, pesticides, pollution, physical inactivity, sleep disruption, smoking) and by pathogens, directly or via olfactory routes to basal-forebrain BBB control centers. The BBB benefits from statins, NSAIDs, estrogen, melatonin, memantine, and the Mediterranean diet. Polymicrobial involvement is supported by upregulation of bacterial, viral, and fungal sensors/defenders in the AD brain, blood, or cerebrospinal fluid. AD serum amyloid-β autoantibodies may attenuate its antimicrobial effects favoring microbial survival and cerebral invasion leading to activation of neurodestructive immune/inflammatory processes, which may also be augmented by age-related immunosenescence. AD may thus respond to antibiotic, antifungal, or antiviral therapy.

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“…These include apocynin [66,67,68], baicalein [69], caffeine [70,71,109], curcumin [72,73,74], niacin [64], nicotine [64], pinocembrin [75,76,110], resveratrol [77,78,79,80,81,111], polyphenols [112], and tanshinone IIA [82,83,84]. However, the number of studies investigating the effects of these agents on neurodegeneration and cognitive performance is limited.…”

Section: Antioxidants Cognitive Decline and Blood-brain Barriermentioning

confidence: 99%

Antioxidants and Dementia Risk: Consideration through a Cerebrovascular Perspective

2016

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A number of natural and chemical compounds that exert anti-oxidative properties are demonstrated to be beneficial for brain and cognitive function, and some are reported to reduce the risk of dementia. However, the detailed mechanisms by which those anti-oxidative compounds show positive effects on cognition and dementia are still unclear. An emerging body of evidence suggests that the integrity of the cerebrovascular blood-brain barrier (BBB) is centrally involved in the onset and progression of cognitive impairment and dementia. While recent studies revealed that some anti-oxidative agents appear to be protective against the disruption of BBB integrity and structure, few studies considered the neuroprotective effects of antioxidants in the context of cerebrovascular integrity. Therefore, in this review, we examine the mechanistic insights of antioxidants as a pleiotropic agent for cognitive impairment and dementia through a cerebrovascular axis by primarily focusing on the current available data from physiological studies. Conclusively, there is a compelling body of evidence that suggest antioxidants may prevent cognitive decline and dementia by protecting the integrity and function of BBB and, indeed, further studies are needed to directly examine these effects in addition to underlying molecular mechanisms.

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Resveratrol Attenuates the Blood-Brain Barrier Dysfunction by Regulation of the MMP-9/TIMP-1 Balance after Cerebral Ischemia Reperfusion in Rats

Cited by 64 publications

References 37 publications

Neurovascular dysfunction and neurodegeneration in dementia and Alzheimer's disease

Neurovascular dysfunction and neurodegeneration in dementia and Alzheimer's disease

Genetic, Transcriptome, Proteomic, and Epidemiological Evidence for Blood-Brain Barrier Disruption and Polymicrobial Brain Invasion as Determinant Factors in Alzheimer’s Disease

Antioxidants and Dementia Risk: Consideration through a Cerebrovascular Perspective

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